While on the neurology floor at the Massachusetts General Hospital, I met several patients who were diagnosed with pseudoseizures, a condition that mimics seizures but is not accompanied by the typical epileptiform EEG findings. This condition is considered today to be psychogenic in etiology. A question came up on rounds one day when a young catatonic patient was admitted to the floor: could there be such a thing as pseudo-catatonia, which might be analogous to pseudoseizures?

Short answer: we don’t know enough about catatonia to be able to separate cases into true catatonia and pseudo-catatonia.

There is no EEG finding specific to catatonia [1]. The underlying pathophysiology is still unclear. Several theories exist, including 1) catatonia is an outward manifestation of intense anxiety (however, not all catatonic patients reported the feeling of anxiety during a catatonic episode), 2) catatonia is primarily a movement disorder caused by dysfunction of GABA binding (some evidence supports this) [2]. Given that there are no objective findings specific to catatonia, however, it is impossible to tease apart potential subtypes other than by using clinical characteristics. Catatonia is currently subcategorized into the retarded type vs. excited type based on clinical presentation.

Diagnosis of catatonia requires at least 3 of the following characteristics (per DSM):

  • Stupor
  • Catalepsy
  • Waxy flexibility
  • Mutism
  • Negativism
  • Posturing
  • Mannerisms
  • Stereotypy
  • Agitation
  • Grimacing
  • Echolalia
  • Echopraxia

Given the diverse combinations of symptoms that are classified under catatonia, it would be very difficult to tease apart true pathophysiological subtypes without objective measures such as EEG or brain imaging findings. Until there are markers for an underlying defect it is difficult to define “true” vs. “pseudo” catatonia.

On the differential diagnosis for catatonia are:

  • Extrapyramidal effects of drugs (i.e. drug-induced parkinsonism) (h/o antipsychotics)
  • Neuroleptic malignant syndrome (h/o antipsychotics)
  • Nonconvulsive status epilepticus (abnormal EEG)
  • Abulia/akinetic mutism (disorders of diminished motivation 2/2 TBI)
  • Locked-in syndrome (MRI abnormality)
  • Vegetative state (h/o severe cerebral injury, abnormal EEG)
  • Stiff person syndrome (antibody testing for GAD65, patient endorses great pain with spasms)

Often times, clinicians will trial benzodiazepines to look for a response. A positive response suggests a diagnosis of catatonia (although stiff person syndrome also shows improvement in response to benzos, and even in up to 40% of cases of catatonia, benzos are ineffective).

References

  1. Carroll BT, Boutros NN. Clinical electroencephalograms in patients with catatonic disorders. Clin Electroencephalogr. 1995;26(1):60-4.
  2. Rasmussen SA, Mazurek MF, Rosebush PI. Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391-398.